European Journal of Cardiovascular Medicine

Postoperative recovery period is well known for complications. Few of them like nausea, vomiting, delirium, confusion may not cause immediate life-threatening situations. However, a few like haemorrhage, cardiac abnormalities, respiratory difficulties, embolism etc that can happen in any post operative case can cause life threatening situations which if not treated timely can result in catastrophic outcomes including death.¹ Amongst these pulmonary related complications are encountered most frequently.

 The overall prevalence of postoperative pulmonary problems varies from 5 percent to as high as 80 percent.² These include pneumonia, pulmonary oedema, thrombosis, atelectasis, bronchospasm, and worsening of pre-existing chronic lung disease.

34 years old, 6 feet tall male was suffering from cholelithiasis and was planned to undergo laparoscopic cholecystectomy. There was no surgical or medical history in the past other than history of occasional cigarette smoking without any significant respiratory symptoms. The patient gave a history of last episode of cigarette smoking 36 hours prior to the scheduled surgery.

He was maintaining 100% oxygen saturation on room air. Systemic examination was within normal limits. Bilateral normal breath sounds were heard on auscultation. Preoperative blood investigations were within normal limits. X-ray chest was reported normal [Figure 1].

A balanced general anaesthesia technique with endotracheal tube with standard monitoring was chosen. Trachea was intubated with an 8.5 mm cuffed endotracheal tube (ET) with black line at the level of vocal cords. Bilateral air entry was confirmed and was equal on auscultation, ET was fixed at 21 cm mark at incisors with tape. End tidal carbon dioxide 2 (Etco2) levels, airway pressures noted and were in within normal limits. Patient was maintained on infusion of iv (intravenous) propofol and iv atracurium. Injection glycopyrrolate 0.2 mg and nalbuphine 6 mg were given as premedication. The insufflation pressures were kept at 10 mm of Hg. Intraoperatively vitals were stable, no significant changes in ventilatory parameters and was uneventful.  The laparoscopic surgery had to be converted to open surgery after about one hour of gas insufflation because of surgical difficulty and concluded safely after two and half hour of intubation. Patient was reversed after muscle recovery Train of four (TOF) 90%. Injection paracetamol 1 g and 100 mg tramadol was administered postoperatively 8 hourly for next 24 hour. He was shifted to the ward postoperatively in a stable pain free state after meeting modified Aldrete score of 9.

On third postoperative day of surgery patient developed mild breathlessness, cough and chest pain on left side of chest, saturation dropped (Spo2 94 % at rest on room air) tachycardia of 106 beats per minute (bpm). On examination there was visible decreased movements on left side of the chest. On auscultation air entry was reduced on left side in upper and lower lobe without any added sound. A differential diagnosis of pulmonary embolism, lung collapse, spontaneous pneumothorax, pneumonitis was considered. Chest x-ray was suggestive of complete collapse of left lung with mediastinum shift towards left side (Figure 2). 2D Echocardiography, D dimers, complete blood count were within normal limits. As his chest x-ray was normal prior to surgery, a diagnosis of atelectasis of lung was made which was confirmed on ultrasound. Fibreoptic Bronchoscopy was planned urgently. Considering the patient stable on oxygen and not deteriorating it was decided that patient be given a chance with good nebulization, postural drainage and good chest physiotherapy for 24 hrs. Patient was kept under strict observation for any deterioration with bronchoscopy team on standby. Patient received humidified oxygen, bronchodilator nebulization and mucolytics. Patient coughed up a black mucous plug after about 4 hours of above. A follow-up chest x-rays revealed lung expansion (Figure 3). Additionally, the patient's clinical condition improved and remained stable, requiring no oxygenation (Spo2 98% at room air).

Figure 1: Preoperative Xray-chest

Figure 2: Third day Xray-chest showing collapsed left lung

Figure 3: Resolution of collapsed lung

The intensive care unit (ICU) and postoperative settings frequently experience acute pulmonary collapse. Endobronchial intubation or tube occlusion due to secretions, blood, or a herniated cuff is one of the most the most common cause.³

Our report highlights the onset of breathlessness associated with considerable pulmonary collapse due to mucus plug on third postoperative day. Various factors which can be responsible for lung collapse in this particular patient are as follows.

Firstly, the most common cause of one lung ventilation in patient who underwent general anaesthesia is endobronchial intubation.  Although bilateral air entry was normal after intubation and there were no such changes in ventilatory parameters which indicate endobronchial intubation. Although anatomical variations can occur but it is highly unlikely that endobronchial intubation occurred in this tall patient.

Second possibility is general anaesthesia itself. There is atelectasis and airway closure in the dependent lung areas during anaesthesia and neuromuscular relaxation, ventilation is redirected to the nondependent lung regions, leading to hypoxemia and elevated alveolar-arterial oxygen gradients.³ Under general anaesthesia, postoperative atelectasis develops 72 hours after surgery. A combination of obstructive and nonobstructive processes is frequently seen in this kind of atelectasis. Ninety percent of individuals receiving general anaesthesia develop atelectasis.⁴

Third possibility is smoking. As the patient was a smoker for 5 years.  Studies show cilia are shorter in healthy smokers than in healthy non-smokers, which is probably a major factor in the reduced mucociliary clearance.⁵ Tobacco smoke-induced mucus hypersecretion, goblet cell hyperplasia, and impaired mucociliary clearance may all be factors in the buildup of luminal mucus.⁶ In smokers with airflow obstruction, goblet cell hyperplasia and hypertrophy are routinely observed in the major airways.⁷. These alterations to goblet cells lead to excessive mucus production and release of mucus production and release of mucus, which eventually accumulates in airway lumen.⁸ Severe mucus plugging can cause breathing difficulties, increased inspiratory pressure.⁹

Fourthly atelectasis can develop as a result of inadequate pain management, which can cause splinting or shallow breathing.¹⁰ The incision was about 5 inches in right subcostal area. Analgesics were administered around the clock and patient had just mild pain according to visual analogue scale (VAS score). Additional causes of abrupt lung collapse include tube kinking, blood clots or foreign bodies. Numerous lung conditions including bronchiectasis, allergic bronchopulmonary aspergillosis, bronchial asthma, cystic fibrosis, and others, have reported significant lung collapse.¹¹

Early ambulation, incentive spirometry, chest physical therapy, tracheal suctioning in intubated patients, positive pressure ventilation, acapella device use, and encouraging patients to take deep breaths have all been demonstrated to reduce atelectasis. These techniques work by temporarily raising transmural pressure, which permits collapsed lung segments to expand again. To get the most benefit preventive measures like incentive spirometry should be taught and implemented prior to surgery and continued in postoperative period till discharge.¹²

Similar case was reported in a 45-year-old woman with a history of asthma and smoking who developed complete left lung and right upper lobe collapse secondary to mucus plugs that developed immediately postoperatively after an uncomplicated reconstructive pelvic surgery was managed conservatively.¹³.

Our observation on the onset of lung collapse in our patient could be because of multiple reasons. Antisialogogue given in this patient could have dried the already present secretions. Endotracheal intubation decreased the natural ability of the body to clear secretions. The insufflation pressures might have affected the lung function as well. The patient was a known smoker. Because in mainstream smoke, about 60% of the particles that are inhaled are deposited., these particles are not entirely removed because long-term smokers' lungs have very high concentrations of them, indicating a significant burden of retained particles.¹⁴ So all these explanation points to the fact that patient may have had secretions in his airways that gathered in their left bronchus before drying out and striking it.

After giving nebulisation with mucolytics and moist oxygen inhalation, these secretions got liquified then expectorated by patient. Ultimately patient developed expansion of left lung. (Figure 3)

Various factors can contribute to the development of atelectasis especially in patient who have undergone general anaesthesia. It is essential to understand and the causes, identify signs and symptoms of postoperative complications. Through preventive measures and timely interventions one can reduce the risk of atelectasis resulting in better outcome.

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